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primary human coronary artery endothelial cells hcaecs  (PromoCell)


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    PromoCell primary human coronary artery endothelial cells hcaecs
    Primary Human Coronary Artery Endothelial Cells Hcaecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 222 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary human coronary artery endothelial cells hcaecs/product/PromoCell
    Average 96 stars, based on 222 article reviews
    primary human coronary artery endothelial cells hcaecs - by Bioz Stars, 2026-06
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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected <t>HCAECs</t> was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.
    Human Coronary Endothelial Cells Hcaecs, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected <t>HCAECs</t> was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.
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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected <t>HCAECs</t> was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.
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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected <t>HCAECs</t> was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.
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    Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells <t>(HCAEC</t> <t>and</t> <t>HCMEC</t> respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.
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    Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells <t>(HCAEC</t> <t>and</t> <t>HCMEC</t> respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.
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    ATCC human coronary artery endothelial cells hcaecs
    Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells <t>(HCAEC</t> <t>and</t> <t>HCMEC</t> respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.
    Human Coronary Artery Endothelial Cells Hcaecs, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected HCAECs was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected HCAECs was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Expressing, Infection, Quantitative RT-PCR, Western Blot

    UK5099 alleviates MRMP-induced mitochondrial damage (A) mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey’s post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: UK5099 alleviates MRMP-induced mitochondrial damage (A) mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey’s post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Infection, Quantitative RT-PCR, Expressing, Western Blot

    UK5099 alleviates MRMP-induced pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay. (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: UK5099 alleviates MRMP-induced pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay. (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay, Expressing, Infection, Western Blot

    MG132-mediated PINK1 deficiency induces mitochondrial damage. (A) Mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E,F) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MG132-mediated PINK1 deficiency induces mitochondrial damage. (A) Mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E,F) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Infection, Quantitative RT-PCR, Expressing, Western Blot

    MG132-mediated PINK1 deficiency induces pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay ( n = 3). (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MG132-mediated PINK1 deficiency induces pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay ( n = 3). (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay, Expressing, Infection, Western Blot

    MPC1 induces pyroptosis of HCAECs via inhibiting PINK1-dependent mitophagy. (A–D) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). (E,F) Cytokine release was determined using ELISA ( n = 3). (G) Cell viability was determined using CCK-8 assay ( n = 3). (H) Cytotoxicity was determined using LDH assay ( n = 3). (I,J) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (K–N) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MPC1 induces pyroptosis of HCAECs via inhibiting PINK1-dependent mitophagy. (A–D) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). (E,F) Cytokine release was determined using ELISA ( n = 3). (G) Cell viability was determined using CCK-8 assay ( n = 3). (H) Cytotoxicity was determined using LDH assay ( n = 3). (I,J) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (K–N) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Expressing, Infection, Western Blot, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay

    Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells (HCAEC and HCMEC respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.

    Journal: Journal of Extracellular Vesicles

    Article Title: The Fatty Acid Transporter CD36 Mediates Uptake, Biodistribution, and Cardioprotection by Small Extracellular Vesicles From HEK293 Cells

    doi: 10.1002/jev2.70254

    Figure Lengend Snippet: Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells (HCAEC and HCMEC respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.

    Article Snippet: HCMEC (human coronary microvascular endothelial cells) and HCAEC (human coronary artery endothelial cells) were cultured in endothelial cell basal medium MV‐2 (PromoCell, C‐22022) supplemented with the supplement mix (PromoCell, C‐39226).

    Techniques: Activity Assay, Incubation, Luciferase